Alcohol Intoxication

Prepared by Dr. Rita Karam

✓Understand the Basics of Alcohol Intoxication

✓Describe the Pharmacokinetics and Metabolism of Alcohol

✓Recognize Clinical Manifestations and Complications

✓Interpret Laboratory and Diagnostic Findings

✓Manage Acute Alcohol Intoxication

✓Address Alcohol Dependence and Withdrawal

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3E. Alcohol Intoxication

Outline
A. Introduction & Background
B. Toxic Alcohols
C. Pharmacokinetics of Ethanol
D. Clinical Manifestations of Ethanol Toxicity
E. Laboratory Studies
F. Emergency Management: Initial Assessment & Supportive Care
G. Tolerance and Alcohol Withdrawal Syndrome
H. Consultations and Complications of Alcohol use and abuse

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A. Introduction and Background
✓Alcohol contributes to chronic diseases, liver failure, and mental health issues.
✓In 2023, 44.5% of liver disease deaths involved alcohol.
✓Alcohol-related issues cost the U.S. $224 billion due to workplace productivity loss,
healthcare expenses, crime, and motor vehicle crashes (CDC 2021)
✓Alcohol Use Disorder (AUD) or Alcoholism: excessive and repetitive consumption of
alcoholic beverages, leading to self-harm or harm to others.
✓The harm may be physical, mental, social, legal, or economic.
✓Because such use is usually considered compulsive, alcoholism is regarded as a disease and
an addiction.
✓BAC = Blood Alcohol Concentration 4
B. Toxic Alcohols

Alcohol Type Common sources Clinical Manifestations Lab Abnormalities

Blurred vision, optic nerve

Glass cleaner fluid (for cars) damage, blindness, hemorrhage
paint remover, photocopying in a deep part of the brain leading Lactic acidosis
Methanol (Oral) fluid, adulterated ethanol to Parkinsonism

Ethylene Glycol Fluorescent urine, calcium Hypocalcemia, wide

(Oral) Antifreeze oxalate crystals QRS, prolonged QT

Propylene Diluent in parenteral Patients with hepatic or renal

Glycol (IV ) medications failure are at higher risk Lactic acidosis

Isopropyl Hand sanitizer, mouthwashes,

Alcohol (Oral antiseptic used for cleaning and May cause acute pancreatitis Acetonemia
and Inhalation) disinfecting
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C. Ethanol Pharmacokinetics
Ethanol is the most commonly consumed type
of alcohol

Absorption: Rapidly absorbed from the

stomach (22%) and small intestine (75%).

Peak Blood Concentration: Reached within

30–90 minutes post-ingestion.

Distribution: Spreads through tissues and body

fluids, including the brain, crosses the
placenta, exposing the fetus.

Metabolism: Mainly in the liver.

Excretion:
✓ Small amounts excreted in the urine
unchanged.
✓ Exhalation: Eliminated through breath (the
basis for breathalyzer tests). 6
C. Ethanol Metabolisme overview

1. Alcohol Dehydrogenase (ADH) Pathway (Major Pathway)

Primary route (~80%) of ethanol metabolism in the liver cytosol.
Converts ethanol → acetaldehyde (toxic) via ADH.
Acetaldehyde is further metabolized by Aldehyde Dehydrogenase (ALDH) into acetate, which enters
circulation for energy.
Normal alcohol consumption
2. Microsomal Ethanol Oxidizing System (MEOS) (CYP2E1 Pathway)
Secondary route (~20%), active in microsomes.
Utilizes CYP2E1 to oxidize ethanol, producing reactive oxygen species (ROS) and free radicals.
Contributes to oxidative stress & liver damage.
Chronic alcohol consumption, as CYP2E1 is induced with prolonged exposure. 7
D. Clinical Manifestations of Ethanol Toxicity

System affected Clinical Effects

Central Nervous System Enhances GABA activity (sedation, impaired coordination, slowed
(CNS) Depression reflexes, slurred speech, poor judgment).
Inhibits Glutamate (confusion, memory loss, unconsciousness).

Hypoglycemia: Blocks glucose production, causing low blood sugar.

Metabolic Effects Acidosis: Excess acetate and ketone production leads to metabolic
acidosis.
Electrolyte imbalances (e.g., low potassium or magnesium)

Cardiovascular Effects Vasodilation (flushed and reddish skin) causes low blood pressure and
hypothermia.
Increased risk of arrhythmias (e.g., atrial fibrillation in binge drinking).
Gastrointestinal & Liver Irritates stomach lining (nausea, vomiting, gastritis).
Effects Chronic use damages the liver (Steatosis - fatty liver, hepatitis, cirrhosis)
.
Respiratory depression: High doses suppress the respiratory center,
Severe Toxicity & Death leading to coma or death.
Multi-organ failure in extreme toxicity

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 F. Laboratory Studies

Test Category
Indications Results/Findings

Most critical test to detect

Serum Glucose All patients
hypoglycemia
Blood Alcohol Helpful in legal cases or severe
Not always required
Concentration (BAC) intoxication
Electrolytes & ABG Suspected metabolic acidosis Anion gap, bicarbonate levels
Toxicology Screen Suicidal ingestion Acetaminophen, salicylates
Suicide attempt or electrolyte
ECG Arrhythmias
imbalance
CBC Chronic alcoholics Anemia, thrombocytopenia
Liver Function Tests
Chronic alcoholics Elevated liver enzymes
(AST/ALT, GGT)
Coagulation Panel Chronic alcoholics with liver
Prolonged clotting time
(PT/INR) disease

Following consumption of any alcohol, the extent of the workup depends partly on the
history and physical examination
Clinical observation is key. Patients can be discharged when they are no longer
intoxicated, regardless of numerical BAC levels
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F. Blood Alcohol Concentration (BAC) Effects

BAC Level Clinical Manifestations

(mg/dL)
Sense of warmth, well-being
< 25
Euphoria, decreased judgment
25-50
Incoordination, ataxia, delayed
50-100 reaction time
100-250 Slurred speech, nystagmus
>250 Coma
Respiratory depression, loss of
>400 protective reflexes, death

A breathalyzer estimates BAC from a breath sample using a

redox reaction. Alcohol is oxidized to acetic acid, generating
a color change or electrical signal, which is then converted
into an estimated BAC.
To pass a breathalyzer test, an individual must have a BAC
level lower than 80mg/dL
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G. Emergency Management – Initial Assessment & Supportive Care

Patients with altered mental status or hemodynamic instability:

1. ABC Approach (Airway, Breathing, Circulation)

2. Monitor blood glucose, electrolytes
3. GI Protection: Proton pump inhibitors (PPIs) may help prevent hemorrhagic
gastritis caused by isopropanol ingestion
4. Adjunctive Therapies and Hemodialysis
5. Antidotal treatment 11
Adjunctive Therapies & Role of Hemodialysis

Adjunctive Therapies:

Ethylene glycol poisoning:

✓ Toxic metabolites: glycolic acid, oxalic acid
✓ Fomepizole (inhibit alcohol dehydrogenase)
✓ Ethanol: competes with methanol or EG for ADH
✓ Sodium Bicarbonate Infusion (for metabolic acidosis)
✓ Thiamine (100 mg IV every 6h) & Pyridoxine (50 mg IV
every 6h) to shift metabolism toward non-toxic
products

Methanol poisoning:
✓ Toxic metabolite: formic acid, which causes optic
nerve damage and acidosis.
✓ Folinic acid (or folic acid) enhances the metabolism of
formic acid to CO₂ and water, helping detoxify it.

When to Consider Hemodialysis?

Hemodialysis is effective but used only when
toxicity is life-threatening or unresponsive to
medical therapy

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Antidotal Therapy for Toxic Alcohols (Methanol
& Ethylene Glycol)

First-Line Antidote: Fomepizole

✓ Inhibit Alcohol Dehydrogenase (ADH)

to block toxic metabolite formation.
✓ Loading dose: 15 mg/kg IV
✓ Maintenance dose: 10 mg/kg IV every
12 hours (for 4 doses)
✓ During Hemodialysis: Additional doses
required
✓ Continue until methanol/ethylene glycol
levels < 20 mg/dL

Alternative Antidote:
Ethanol (if fomepizole unavailable)
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 H. Tolerance and Alcohol Withdrawal Syndrome

Chronic alcohol use leads to tolerance and physical dependence. Stopping suddenly can
trigger withdrawal symptoms such as anxiety, hallucinations, seizures and delirium tremens.

Delirium tremens is a severe and life-threatening alcohol withdrawal syndrome marked by

confusion, agitation, hallucinations, tremors, and autonomic instability typically occurring
2–3 days after stopping heavy drinking. 14
 Disulfiram and Acamprosate for Alcoholism Treatment

Disulfiram (Antabuse*) is used to treat alcohol use disorder by causing unpleasant effects
when alcohol is consumed.
It is a deterrent or aversion agent. It works by blocking AlDH leading to acetaldehyde buildup.
It causes unpleasant reactions (like nausea and flushing) when alcohol is consumed,
discouraging drinking
Acamprosate (Aotal*) is a craving-reduction agent. It is used to support long-term abstinence
in individuals with alcohol dependence. It helps reduce cravings and prevent relapse by
balancing Glutamate and GABA activity in the brain. It is safe if alcohol is consumed, but it
may be less effective.
Marketed in Lebanon. Manufactured by Biogaran-France 15
I. Consultations and Complications of Alcohol use and abuse
Consultations
Referral to an alcohol detoxification facility for patients with dependence or abuse.
Toxicology consultation for suspected cases of Toxic alcohol ingestion
Complications
Fetal Alcohol Syndrome (FAS)
A severe disorder caused by prenatal alcohol exposure, leading to growth deficiencies,
facial abnormalities, and neurodevelopmental impairments:
Due to disruption of normal brain development: including impairments in attention,
reaction time, executive functions, motor skills, memory, language, social and adaptive
functions, and reduced IQ
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